Electrolytes Flashcards

1
Q

Potassium
Intracellular or Extracellular
Hormones affecting

A

Intracellular

Insulin and Adrenaline (B agonists) move K intracellular
Aldosterone moves into collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why do ACE inhibitors cause hyperkalemia

A

ACE converts Angiotensin I to Angiotensin II which increases the release of aldosterone from the adrenal cortex = Less K excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of hyperkalemia (5)

A

Renal causes: AKI, Chronic kidney disease, Type 4 RTA eg Diabetic nephropathy

Drugs: ACEi/ARBs, Beta-blockers, NSAIDs, K+ sparing diuretics eg Spironolactone, Heparin, etc
Mineralocorticoid deficiency (Addison’s disease)

Exogenous K - Supplements, bananas

Endogenous K - Tumour lysis syndrome, Rhabdomyolysis, trauma, burns.

Shift from intracellular to extracellular space - Acidosis e.g. DKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ECG changes in hyperkalaemia

A
Tall tented T waves
Long PR
Flat P waves
Broad QRS
Sine waves - Late sing. Cardiac arrest imminent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Symptoms of hyperkalaemia.

A
Often asymptomatic
Palpitations/ chest pain
Bradycardia/ Heart block
Tachypnoea
Muscular weakness/ paralysis
Generalized weakness/ fatigue
Depressed tendon reflexes
Cardiac arrest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Management of hyperkalaemia

A

For K+ 5.5 – 6.0 mmol/L: Stop K sparing drugs and
restrict dietary or IV potassium intake.

K+ 6.0 – 6.5 mmol/L with no ECG Changes: Oral Calcium Resonium 15g 3-4 times a
day in water. Prescribe lactulose 10-20 ml qds with
it. It takes around 10 hours for effect.

K+> 6.5 mmol/L or >6.0 mmol/L
with ECG Changes - 10ml 10% calcium gluconate IV over 5 minutes.
Insulin IV &; Salbutamol nebs drives K into cells+ 50ml 50% dextrose.
Use central access if available, otherwise use a large
peripheral vein.
Look for normalisation of ECG on cardiac monitor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ECG changes in hypokalaemia

A

Flattened & inverted T waves;
Increased amplitude and width of the P wave
Prolongation of the PR interval
ST depression
Prominent U waves
Arrhythmias: VT, VF, Torsades de Pointes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypokalaemia features

A

Often asymptomatic until arrest.

Weakness, fatigue, constipation, muscle cramping, palpitations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of hypokalaemia

A

Decreased intake: anorexia nervosa,
malnutrition, chronic alcoholism,
inappropriate IV therapy.

Transcellular shift: insulin, beta-agonists,
theophylline, re-feeding syndrome.

Renal loss: diuretic therapy, mineralocorticoid
excess/therapy, aminoglycosides, alkalosis,
renal tubular acidosis, magnesium depletion.

Extrarenal loss: Chronic D&V, laxative abuse,
fistula, villous adenoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Extra renal loss vs renal loss

A

Urine potassium < 10 indicates extra-renal loss, urine
potassium > 20 indicates renal loss.

Nb. If extra-renal K+ loss (e.g. vomiting /diarrhoea)
is associated with dehydration this can stimulate
aldosterone release which will increase renal K+ loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Management of hypokalaemia

A

Treat the cause, in general oral K+ is
preferred. In severe and potential life threatening
hypokalaemia the rate of K+ infusion should not
exceed 20 mmol/h.

If secondary to low Mg then give Mg replacement –
otherwise potassium may be refractory to treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Management of Hypomagnesemia

A

≤ 0.5 mmol/L - IV infusion (peripheral or central) magnesium sulphate 20 mmol
(5g) in 500 ml 0.9% saline or 5% dextrose over 12
hours for 3-5 days.

With life threatening symptoms ( e.g seizures,
arrhythmias): IV bolus of 8mmol MgSO4 (2g) over
10-15 minutes followed by infusion as stated above.

Nb. Mg can accumulate in the kidneys so needs to be reduced and monitored in CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Maintenance requirements
Water
Na
K

A

20-25ml/kg/day
1mmol/kg/day
1mmol/kg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Features of hyponatraemia

A

Rarely occur below 120mmol/L
Result from movement of water into brain cells causing cerebral oedema
Headache, confusion, convulsions and coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of hyponatraemia

A

Dilutional - Heart failure, liver failure, renal failure, hypoalbuminaemia

Hypovolemia (Determine difference by Na in urine)

  • Renal - Diuretics, Osmotic diuresis (hyperglycemia), adrenocortical insufficiency.
  • Extra renal - Haemorrhage, vomiting, burns, diarrhoea.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Magnesium and potassium levels in hyponatraemia

A

Must be checked as low levels can stimualte ADH release and cause a dilutional hyponatrraemia

17
Q

Central pontine myelinolysis

A

Areas of demyelination causing quadriparesis, respiratory arrest, pseudobulbar palsy, mutisum and seizures.
Caused by rapid overcorrection of Na

18
Q

Management of hyponatremia resulting from water excess

A

Treat underlying cause
Restrict fluid to 1L and review diuretics

Acute hyponatraemia with neurological symptoms

  • Infuse hypertonic saline (3%) at a rate of 1-2ml/kg/hour
  • Aim to raise Na by 8-10 mols in the first day and 8 mols /day therafter
  • Frusimide to encourage excretion of free water.
  • Hypertonic saline is CI in fluid overload - Instead give mannitol
19
Q
Hypernatraemia 
What
Causes
Features
Management
A

> 145mmol/L

Poor intake of water or water loss in excess sodium

Nausea, vomiting, fever, confusion

If mild correct over 48 hours with 5% Dex. If severe >170mmol - Correct with normal saline.

20
Q
Hypomagnesaemia 
Causes
Effect on K
Effect on PTH
Features
Management
A

GI loss of Mg - Diarrhoea, malabsorption, bowel ressection (Most common)
Renal loss - Osmotic diuresis in DM, diuretics, alcohol abuse.

Increases renal K excretion (Hypokalaemia)
Inhibits PTH (Hypocalcaemia)

Features related to hypokalaemia & hypocalcaemia

Oral supplements

21
Q

Hypermagnesaemia

A

Rare and usually Iatrogenic occuring in patient with renal failure who have been given Mg containing antacids or laxatives.

22
Q

Hypercalaemia
Usual cause
Other causes

A

Primary hyperparathyroidism or malignancy (Bone mets/multiple myeloma)
Nb if severe >3.5mmol cause is likely malignancy

Thyrotoxicosis, Addisons disease, excess vit D
Drugs - Thiazides - Reduced renal tubular excretion, Lithium - Increased PTH production.

23
Q

Features of hypercalcaemia

A

Abdominal groans - Anorexia, nausea and vomiting, abdo pain, PUD, acute pancreatitis
Thrones - Polyuria, polydipsia, dehydration.
Stones - if long standing- Renal colic
Psychic overtones - Depression, dementia, confusion, memory
Muscle + CVS - Weakness, proximal myopathy, fatigue
HTN, *short QT

24
Q

Ix of hypercalcaemia

A

High corrected Ca (<3 = PHPT, >3 = malignancy)
Albumin - high -> with high urea = dehydration
Alk phos - normal in myeloma (unless fracture healing), raised in bony mets
Calcitonin - B cell lymphoma
PTH - high = PHPT, low = granulomatous or adrenal
*XR - bone abnormalities, cysts, pathological fractures etc

25
Management of hypercalcaemia
Acute >3.5 0.9% saline - hydration and increase urinary excretion Loop diuretic - furosemide for fluid overload Post rehydration - IV bisphosphonates - pamidronate or zoledronic acid If vit D toxicity, sarcoid, lymphoma - glucocorticoids If secondary HPT = cinacalcet If underlying kidney disease - haemodialysis
26
Causes of hypocalcaemia (4)
CKD (most common) resulting from reduced vit D secretion and phosphate retention. Hypomagnesaemia (inhibits PTH) Parathyroid sugery/radio Vitamin D deficiency
27
Hypocalcaemia Symptoms Signs
Paresthesia: fingers, toes, mouth Tetany (emergency) Carpopedal spasm (wrist flexion and fingers drawn together) Muscle cramps Chvostek’s sign - latent tetany Tap facial nerve face spasms Trousseua’s sign - from increased neuromuscular excitability Inflate a BP cuff above systolic - look for carpopedal spasm Seizures Prolonged QT (shortened in hyperCa)
28
Management of hypocalcaemia
Acute: seizures/tetany or <1.9 10ml 10% calcium gluconate slow IV infusion, repeat as necessary Oral calcium Monitor Ca If hypomagnesaemia - correct otherwise Ca will not respond Chronic: Ca and vit D
29
Osmolality calculation | Use in Hyponatraemia
2xNa + urea + Glucose For true hyponataemia there must be a deficit in serum osmolality. If Normal osmolality = High triglycerides, High total protein If High = Hyperglycaemia
30
ALT vs ALP
ALT is found in high concentrations within hepatocytes and enters the blood following hepatocellular injury. It is, therefore, a useful marker of hepatocellular injury. ALP is particularly concentrated in the liver, bile duct and bone tissues. ALP is often raised in liver pathology due to increased synthesis in response to cholestasis. As a result, ALP is a useful indirect marker of cholestasis. A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP = hepatocellular injury A less than 10-fold increase in ALT and a more than 3-fold increase in ALP = cholestasis
31
Causes of isolated rise in ALP
Bony metastases / primary bone tumours (e.g. sarcoma) Vitamin D deficiency Recent bone fractures Renal osteodystrophy
32
If there is a rise in ALP? Another test? If raised as well? If not raised?
GGT Suggestive of biliary epithelial damage and bile flow obstruction. It can also be raised in response to alcohol and drugs such as phenytoin. Non-hepatobiliary pathology. Alkaline phosphatase is also present in bone and therefore anything that leads to increased bone breakdown can elevate ALP.
33
Assessing liver function tests (4)
Serum bilirubin Serum albumin Prothrombin time (PT) Serum blood glucose
34
Using stool and urine to determine cause of jaundice
Normal urine + normal stools = pre-hepatic cause Dark urine + normal stools = hepatic cause Dark urine + pale stools = post-hepatic cause (obstructive)
35
ALT:AST ratio
ALT > AST is seen in chronic liver disease | AST > ALT is seen in cirrhosis and acute alcoholic hepatitis
36
Anion Gap Calculation High Normal
K+Na - Cl+Hco3 If the anion gap is raised, this suggests that there is increased production, or reduced excretion, of fixed/ organic acids e.g. Lactic acid (sepsis, tissue ischaemia) Urate (renal failure) Ketones (diabetic ketoacidosis) Drugs/ toxins (salicylates, methanol, ethylene glycol) ``` If there is a metabolic acidosis with a normal anion gap, then this is either due to loss of bicarbonate, or accumulation of H+ ions. Causes include: Renal tubular acidosis Diarrhoea Addison's disease Pancreatic fistula ```